Prevalence and Correlates of Hepatitis C Infection among Male Injection Drug Users in Detention, Tehran, Iran

For the benefit of planning for the future care and treatment of people infected with hepatitis C virus (HCV) and to help guide prevention and control programs, data are needed on HCV seroprevalence and associated risk factors. We conducted a cross-sectional sero-behavioral survey of injection drug users (IDU) detained for mandatory rehabilitation during a police sweep of Tehran, Iran, in early 2006. During the study period, a consecutive sample comprising 454 of 499 (91.0%) men arrested and determined to be IDU by urine test and physical examination consented to a face-to-face interview and blood collection for HCV antibody testing. Overall, HCV prevalence was 80.0% (95% confidence interval (CI) 76.2–83.6). Factors independently associated with HCV infection included history of incarceration (adjusted OR 4.35, 95% CI 1.88–10.08), age of first injection ≤25 years (OR 2.72, 95% CI 1.09–6.82), and history of tattooing (OR 2.33, 95% CI 1.05–5.17). HCV prevalence in this population of IDU upon intake to jail was extremely high and possibly approaching saturation. Findings support that incarceration is contributing to the increased spread of HCV infection in Iran and calls for urgent increased availability of HCV treatment, long-term preparation for the care of complications of chronic infection, and rapid scale-up of programs for the primary prevention of parenterally transmitted infections among drug users

Responsible Governance for Mental Health Research in Low Resource Countries

Blurb: Taghi Yasamy and colleagues identify challenges facing good research governance in low- and middle-income countries and provide suggestions for a way forward

Responsible Governance for Mental Health Research in Low Resource Countries

Blurb: Taghi Yasamy and colleagues identify challenges facing good research governance in low- and middle-income countries and provide suggestions for a way forward

Serum estrogen levels and prostate cancer risk in the prostate cancer prevention trial: a nested case–control study

OBJECTIVE: Finasteride reduces prostate cancer risk by blocking the conversion of testosterone to dihydrotestosterone. However, whether finasteride affects estrogens levels or change in estrogens affects prostate cancer risk is unknown. METHODS: These questions were investigated in a case-control study nested within the prostate cancer prevention trial (PCPT) with 1,798 biopsy-proven prostate cancer cases and 1,798 matched controls. RESULTS: Among men on placebo, no relationship of serum estrogens with risk of prostate cancer was found. Among those on finasteride, those in the highest quartile of baseline estrogen levels had a moderately increased risk of Gleason score < 7 prostate cancer (for estrone, odds ratio [OR] = 1.51, 95% confidence interval [CI] = 1.06-2.15; for estradiol, OR = 1.50, 95% CI = 1.03-2.18). Finasteride treatment increased serum estrogen concentrations; however, these changes were not associated with prostate cancer risk. CONCLUSION: Our findings confirm those from previous studies that there are no associations of serum estrogen with prostate cancer risk in untreated men. In addition, finasteride results in a modest increase in serum estrogen levels, which are not related to prostate cancer risk. Whether finasteride is less effective in men with high serum estrogens, or finasteride interacts with estrogen to increase cancer risk, is uncertain and warrants further investigation

Candidate pathways and genes for prostate cancer: a meta-analysis of gene expression data

<p>Abstract</p> <p>Backgound</p> <p>The genetic mechanisms of prostate tumorigenesis remain poorly understood, but with the advent of gene expression array capabilities, we can now produce a large amount of data that can be used to explore the molecular and genetic mechanisms of prostate tumorigenesis.</p> <p>Methods</p> <p>We conducted a meta-analysis of gene expression data from 18 gene array datasets targeting transition from normal to localized prostate cancer and from localized to metastatic prostate cancer. We functionally annotated the top 500 differentially expressed genes and identified several candidate pathways associated with prostate tumorigeneses.</p> <p>Results</p> <p>We found the top differentially expressed genes to be clustered in pathways involving integrin-based cell adhesion: integrin signaling, the actin cytoskeleton, cell death, and cell motility pathways. We also found integrins themselves to be downregulated in the transition from normal prostate tissue to primary localized prostate cancer. Based on the results of this study, we developed a collagen hypothesis of prostate tumorigenesis. According to this hypothesis, the initiating event in prostate tumorigenesis is the age-related decrease in the expression of collagen genes and other genes encoding integrin ligands. This concomitant depletion of integrin ligands leads to the accumulation of ligandless integrin and activation of integrin-associated cell death. To escape integrin-associated death, cells suppress the expression of integrins, which in turn alters the actin cytoskeleton, elevates cell motility and proliferation, and disorganizes prostate histology, contributing to the histologic progression of prostate cancer and its increased metastasizing potential.</p> <p>Conclusion</p> <p>The results of this study suggest that prostate tumor progression is associated with the suppression of integrin-based cell adhesion. Suppression of integrin expression driven by integrin-mediated cell death leads to increased cell proliferation and motility and increased tumor malignancy.</p